Vadasz Z, Misselevich I, Norman D, Peled E, Boss J H
The Pediatric Hematology-Oncology Unit, Bnai-Zion Medical Center, Haifa 31048, Israel.
Exp Mol Pathol. 2004 Oct;77(2):145-8. doi: 10.1016/j.yexmp.2004.06.002.
The expedited revascularization of the rats' avascular, necrotic femoral heads suggests the operation of angiogenic factor(s). The blood circulation of the epiphysis was interrupted by cutting the cervical periosteum and the ligamentum teres of rats' femoral heads. Three days postoperatively, the marrow was necrotic. Seven days postoperatively, the subchondral bony plate and trabecular bone were necrotic as well. The joint capsule was distended by myriad, so-called synovial fibroblasts, all of which were virtually immunoreactive with an antibody to vascular endothelial growth factor. The expression of this factor in the synovial membrane of non-operated rats was limited to preexisting blood vessels. Revascularization of necrotic, avascular femoral heads makes up the essential step in the chain of events terminating in the repair processes, that is, resorption of the necrotic debris and its substitution by newly formed bony and hematopoietic-fatty tissues. Synthesis and release of excessive amounts of vascular endothelial growth factor by these fibroblasts explain the lively angiogenesis in the necrotic intertrabecular spaces of the femoral heads.
大鼠缺血性坏死股骨头的快速血管再生提示血管生成因子的作用。通过切断大鼠股骨头的颈周骨膜和圆韧带,使骨骺的血液循环中断。术后3天,骨髓坏死。术后7天,软骨下骨板和小梁骨也坏死。关节囊被大量所谓的滑膜成纤维细胞扩张,所有这些细胞实际上都能与血管内皮生长因子抗体发生免疫反应。该因子在未手术大鼠滑膜中的表达仅限于已有的血管。坏死缺血性股骨头的血管再生是导致修复过程(即坏死碎片的吸收及其被新形成的骨组织和造血脂肪组织替代)的一系列事件中的关键步骤。这些成纤维细胞合成并释放过量的血管内皮生长因子,解释了股骨头坏死小梁间隙中活跃的血管生成现象。